Different mechanisms have been investigated to explain the potential protective effects of Gln against inflammatory injury, such as: attenuation of excessive NF-κB activation reducing the release of TNF-α, IL-6, and IL-18 in sepsis [11]; up regulation of HSP70 and HSP72 [12-17] repairing denaturated/injured proteins or promoting their degradation following irreparable injury; and increment in tissue glutathione levels, improving the antioxidant status [37]. This evidence concerns the gene NFKB1 and Sepsis.